AIIMS NOV 2007 Exam Recalls

All of the following can be used for thromboprophylaxis except:
a. Heparin
b. Aspirin
c. Warfarin
d. Antithrombin-III

ANS: D

Primary Prophylaxis
The most effective way to reduce the mortality associated with PE and the morbidity associated with the postthrombotic syndrome is to institute primary prophylaxis in patients at risk for VTE. On the basis of well-defined clinical criteria, patients can be classified as being at low, moderate, or high risk for VTE, and the choice of prophylaxis should be tailored to the patient's risk [see Table 6]. In the absence of prophylaxis, the frequency of fatal postoperative PE ranges from 0.1% to 0.4% in patients undergoing elective general surgery and from 0.4% to 5% in patients undergoing elective hip or knee surgery, emergency hip surgery or surgery for major trauma or spinal cord injury. Prophylaxis is cost-effective for most high-risk groups.68
Prophylaxis is achieved either by modulating activation of blood coagulation or by preventing venous stasis by using the following proven approaches: low-dose subcutaneous heparin, intermittent pneumatic compression of the legs, coumarin anticoagulants, adjusted doses of subcutaneous heparin, graduated compression stockings, LMWHs, or fondaparinux.61,68 Antiplatelet agents, such as aspirin, also prevent VTE but are less effective than the previously stated methods.68,69
[ACP MEDICINE 2007]

95. When a person changes position from standing to lying down position, following occurs:
a. Heart rate increases and settles at a higher level
b. Venous return to the heart rises immediately
c. Cerebral blood flow becomes more than that in standing position and settles at a higher level
d. Decrease in blood flow to the lung apex

I could not find any direct refrence but below is some indirect refrence

answer b.venous retrun to heart increases immediately

Guyton Physiology 11th edition page 287

Treatment by the Head-Down Position.

When the pressure
falls too low in most types of shock, especially in
hemorrhagic and neurogenic shock, placing the patient
with the head at least 12 inches lower than the feet
helps tremendously in promoting venous return,
thereby also increasing cardiac output.
This headdown
position is the first essential step in the treatment
of many types of shock

The diagnosis of hydatid disease can be strongly suggested by the results of radiographic studies.113,116 Plain films detect pulmonary cysts117 but often do not visualize cysts in other organs unless they are calcifiedâ€”a process that occurs mostly in hepatic cysts. On CT and MRI, echinococcal cysts appear as well-defined, thick- or thin-walled cysts that may have calcified rims.116,117,118 In older lesions, where scolices and daughter cysts form hydatid sand that settles in the dependent portion of the cyst, a layer of fluid can be visualized. Dependent movement of calcified hydatid sand, on repositioning and ultrasound monitoring, is strongly suggestive, if not pathognomonic, of a hydatid cyst. A pathognomonic CT finding in intact cysts is the presence of daughter cysts that are either free within the cyst or adherent to the inner germinal layer. Separation and collapse of cyst wall layers and the introduction of air into the space between the layers can be detected on plain films (as the meniscus, double arch, or water lily signs) and by CT scan.

A patient presents with Carcinoma of the larynx involving the left false cords, left arytenoids and the left aryepiglottic folds with bilateral mobile true cords. Treatment of choice is:
a. Vertical hemilaryngectomy
b. Horizontal hemilaryngectomy
c. Radiotherapy followed by chemotherapy
d. Total laryngectomy

Answer b.horizontal hemilaryngectomy

Refrence bailey and Johnson head and neck surgery and otolaryngology 4th edition 2006

Two basic types of supracricoid partial laryngectomy (SCPL) exist: one in which the epiglottic and preepiglottic space are resected, and one in which they are spared. In both cases, both true and false cords and the entire thyroid cartilage are resected, and at least one arytenoid cartilage must be spared. For glottic carcinoma a procedure is used in which the epiglottis and preepiglottic space are spared and the space is reconstructed by suturing the cricoid cartilage to the epiglottis and hyoid bone and tongue base; this procedure is known as a cricohyoidoeopiglottopexy (CHEP). A procedure in which the epiglottis and preepiglottic space are resected is used for supraglottic and transglottic carcinomas in which this space is reconstructed by suturing the cricoid cartilage to the hyoid and tongue base: this procedure is known as a cricohyoidopexy (CHP) (1, 2).
The open supraglottic partial laryngectomy (SGPL) is performed by resecting the upper portion of the thyroid cartilage, the epiglottis and preepiglottic space, and the false cords. The hyoid bone is resected only if it is involved by carcinoma. The reconstruction, known as a thyrohyoidopexy (THP), is performed by suturing the thyroid cartilage to the hyoid and tongue base. The difference between the SCPL with CHP and the SGPL alone is that in the SCPL with CHP the entire thyroid cartilage and the true cords are resected. The SGPL is used for selected supraglottic carcinomas (3).

This chapter focuses on early glottic and supraglottic carcinomas (T1N0 and T2N0), which can be treated either with SCPL with CHEP or CHP and those that can be treated with SGPL alone

Another important concept is the idea of the cricoarytenoid unit (Fig. 121C.3). In the conservation surgery paradigm, in which the accepted open partial laryngectomies were the vertical partial laryngectomy and the open SGPL, the main focus was on the vocal cord itself. With the transition to the organ preservation surgery paradigm, which includes SCPL as well as the tranoral laser techniques, the focus shifts to the cricoarytenoid unit. The cricoarytenoid unit is considered the fundamental functional unit of the larynx. It includes one arytenoid cartilage with its associated cricoarytenoid musculature and recurrent and superior laryngeal nerves. Preservation of one cricoarytenoid unit with the associated cricoid ring allows for speech and swallowing without a permanent tracheostomy

The SCPL and SGPL are fundamentally similar procedures (Fig. 121C.4, 121C.5, 121C.6, 121C.7, 121C.8, 121C.9, 121C.10, 121C.11, 121C.12, 121C.13, 121C.14 and 121C.15). They are all horizontal partial laryngectomieswhich means that entry into the

larynx and exposure of the cancer before resection is via a horizontal laryngotomy, either just below the hyoid bone as in the case of SGPL and SCPL with CHP, or just above the false cords as in the case of the SCPL with CHEP.

If we limit our discussion to T1N0 and T2N0 supraglottic carcinomas, then OPS, including endoscopic laser supraglottic partial laryngectomy, open supraglottic laryngectomy, and supracricoid partial laryngectomy can be expected to have local control in the 90% range, whereas with radiation therapy alone the local control is approximately 20% less (3, 8, 11, 20, 21, 22, 23, 24). In addition, as with glottic carcinoma, Parsons et al. (25) noted a 5-year survival of 30% in patients who failed locally after radiation therapy for all T stages of supraglottic carcinoma.
Currently, SGPL as a surgical option is limited because of the advent of transoral laser SGPL. This is because comparable local control rates are seen for open versus transoral laser SGPL. In addition, a decrease was seen in acute morbidity following transoral laser SGPL by avoiding a tracheostomy in almost all cases in which the transoral approach was used, as well as faster swallowing rehabilitation following the transoral approach. The only indication for currently using open SGPL for T1 or T2 supraglottic carcinoma are cases in which the head and neck Anatomy precludes endoscopic exposure of the larynx adequate for transoral laser SGPL. The oncologic contraindications include (a) cricoid or thyroid cartilage invasion; (b) cancer invasion of the mucosa of the arytenoid cartilage; (c) cancer invasion of the posterior or anterior commissure; (d) impaired mobility or fixation of the vocal cord; (e) malignant invasion of the base of the tongue closer than 1 cm to the circumvallate papillae; (f) impaired motion of the tongue base, indicating deep cancer invasion; and (g) invasion of the floor of the mouth in carcinomas with vallecular involvement.Although a variety of technical maneuvers have been forwarded to quantify â€œexposureâ€ during laryngoscopy, the practical approach is to perform a separate endoscopy at which time a percutaneous gastrostomy, if indicated, can also performed. At that time, the surgeon can also assess whether the larynx can be adequately exposed for the transoral laser SGPL, which is scheduled for a subsequent surgical date. If the patient's larynx cannot be exposed adequately for transoral laser SGPL, then an open SGPL can be performed at the later date. Closed laryngoscopes do not allow for adequate exposure of the supraglottis for laser resection, with the exception of the occasional use of the Lindholm scope (Storz, Tuttlingen, Germany). Rudert (26) modified the bivalving laryngoscope originally described by Weerda et al. (27) into a Storz supraglottiscope in which the lateral plates of its spatulas can be positioned to keep the border of the tongue obscuring the operative field.
The SCPL with CHP is used for selected T2 supraglottic carcinomas that have extension from the supraglottis to the glottic level (1).
The oncologic contraindications for SCPL with CHP include (a) arytenoid cartilage fixation; (b) infraglottic extension of tumor more than 15 mm anteriorly (cricothyroid membrane), more than 5 mm posterolaterally, or reaching the superior border of the cricoid cartilage; (c) extensive preepiglottic space invasion with clinical evidence of bulging beneath the vallecula mucosa or extension through the thyrohyoid membranes; (d) tumor abutting the hyoid bone that would require resection of this bone; (e) cricoid cartilage invasion; (f) involvement of the pharynx or interarytenoid fixation; and (g) external thyroid cartilage perichondrial invasion and extralaryngeal spread of tumor. Expected local control rates for SCPL with CHP are in the 90% range (28).

so from this following things can be understood

1)hemilarynectomy is c?I if both aretynoid in included not singe(one function cricoarytenoid unit)

2)single areytenoid involvement in contra indication for endoscopic surgery and not sgpl

True about fibrates is all except:
a. (MOA)â€¦.PPARαâ€¦.lipoprotein lipaseâ€¦decreased LDLâ€¦
b. Absorped better on empty stomach and decreased on food intake
c. Side effects include rash, myalgia, impotence and many others
d. They are the drug of choice in type III hyperlipidemia and

Despite extensive studies in humans, the mechanisms by which fibrates lower lipoprotein levels, or raise HDL levels, remain unclear (Illingworth, 1991). Recent studies suggest that many of the effects of these compounds on blood lipids are mediated by their interaction with peroxisome proliferator activated receptors (PPARs) (Kersten et al., 2000), which regulate gene transcription. Three PPAR isotypes (a, b, and g) have been identified. Fibrates bind to PPARa, which is expressed primarily in the liver and brown adipose tissue and to a lesser extent in kidney, heart, and skeletal muscle. Fibrates reduce triglycerides through PPARa-mediated stimulation of fatty acid oxidation, increased LPL synthesis, and reduced expression of apoC-III. An increase in LPL would enhance the clearance of triglyceride-rich lipoproteins. A reduction in hepatic production of apoC-III, which serves as an inhibitor of lipolytic processing and receptor-mediated clearance, would enhance the clearance of VLDL. Fibrate-mediated increases in HDL-C are due to PPARa stimulation of apoA-I and apoA-II expression (Staels and Auwerx, 1998), which increases HDL levels. Fenofibrate is more effective than gemfibrozil at increasing HDL levels (Rader, 2003).

LDL levels rise in many patients treated with gemfibrozil, especially those with hypertriglyceridemia. However, LDL levels are unchanged or fall in others, especially those whose triglyceride levels are not elevated or who are taking a second-generation agent, such as fenofibrate, bezafibrate, or ciprofibrate. The decrease in LDL levels may be due in part to changes in the cholesterol and triglyceride contents of LDL that are mediated by CETP; such changes can alter the affinity of LDL for the LDL receptor. There also is evidence that a PPARa-mediated increase in hepatic SREBP-1 production enhances hepatic expression of LDL receptors (Kersten et al., 2000). Lastly, fibrates reduce the plasma concentration of small, dense, more easily oxidized LDL particles (Yuan et al., 1994; Vakkilainen et al., 2003).

Most of the fibric acid agents have potential antithrombotic effects, including inhibition of coagulation and enhancement of fibrinolysis. These salutary effects also could alter cardiovascular outcomes by mechanisms unrelated to any hypolipidemic activity (Watts and Dimmitt, 1999).

Effects on Lipoprotein Levels. The effects of the fibric acid agents on lipoprotein levels differ widely, depending on the starting lipoprotein profile, the presence or absence of a genetic hyperlipoproteinemia, the associated environmental influences, and the specific fibrate used.

Patients with type III hyperlipoproteinemia (dysbetalipoproteinemia) are among the most sensitive responders to fibrates (Mahley and Rall, 2001). Elevated triglyceride and cholesterol levels are dramatically lowered, and tuberoeruptive and palmar xanthomas may regress completely. Angina and intermittent claudication also improve (Kuo et al., 1988).

In patients with mild hypertriglyceridemia (e.g., triglycerides <400 mg/dl), fibrate treatment decreases triglyceride levels by up to 50% and increases HDL-C concentrations about 15%; LDL-C levels may be unchanged or increase. The second-generation agents, such as fenofibrate, bezafibrate, and ciprofibrate, lower VLDL levels to a degree similar to that produced by gemfibrozil, but they also are more likely to decrease LDL levels by 15% to 20%. In patients with more marked hypertriglyceridemia (e.g., 400 to 1000 mg/dl), a similar fall in triglycerides occurs, but LDL increases of 10% to 30% are seen frequently. Normotriglyceridemic patients with heterozygous familial hypercholesterolemia usually experience little change in LDL levels with gemfibrozil; with the other fibric acid agents, reductions as great as 20% may occur in some patients.

Fibrates usually are the drugs of choice for treating severe hypertriglyceridemia and the chylomicronemia syndrome. While the primary therapy is to remove alcohol and as much fat from the diet as possible, fibrates help both by increasing triglyceride clearance and by decreasing hepatic triglyceride synthesis. In patients with chylomicronemia syndrome, fibrate maintenance therapy and a low-fat diet keep triglyceride levels well below 1000 mg/dl and thus prevent episodes of pancreatitis.

In a 5-year study of hyperlipidemic men, gemfibrozil reduced total cholesterol by 10% and LDL-C by 11%, raised HDL-C levels by 11%, and decreased triglycerides by 35% (Frick et al., 1987). Overall, there was a 34% decrease in the sum of fatal plus nonfatal cardiovascular events without any effect on total mortality. No increased incidence of gallstones or cancers was observed. Subgroup analysis suggested that the greatest benefit occurred in the subjects with the highest levels of VLDL or combined VLDL and LDL and in those with the lowest HDL-C levels (<35 mg/dl). Gemfibrozil may have affected the outcome by influencing platelet function, coagulation factor synthesis, or LDL size. In a recent secondary prevention trial, gemfibrozil reduced fatal and nonfatal CHD events by 22% despite a lack of effect on LDL-C levels. HDL-C levels increased by 6%, which may have contributed to the favorable outcome (Rubins et al., 1999).

Absorption, Fate, and Excretion. All of the fibrate drugs are absorbed rapidly and efficiently (>90%) when given with a meal but less efficiently when taken on an empty stomach. The ester bond is hydrolyzed rapidly, and peak plasma concentrations are attained within 1 to 4 hours. More than 95% of these drugs in plasma are bound to protein, nearly exclusively to albumin. The half-lives of fibrates differ significantly (Miller and Spence, 1998), ranging from 1.1 hours (gemfibrozil) to 20 hours (fenofibrate). The drugs are widely distributed throughout the body, and concentrations in liver, kidney, and intestine exceed the plasma level. Gemfibrozil is transferred across the placenta. The fibrate drugs are excreted predominantly as glucuronide conjugates; 60% to 90% of an oral dose is excreted in the urine, with smaller amounts appearing in the feces. Excretion of these drugs is impaired in renal failure, though excretion of gemfibrozil is less severely compromised in renal insufficiency than is excretion of other fibrates (Evans et al., 1987). Nevertheless, the use of fibrates is contraindicated in patients with renal failure.

Adverse Effects and Drug Interactions. Fibric acid compounds usually are well tolerated (Miller and Spence, 1998). Side effects may occur in 5% to 10% of patients but most often are not sufficient to cause discontinuation of the drug. Gastrointestinal side effects occur in up to 5% of patients. Other side effects are reported infrequently and include rash, urticaria, hair loss, myalgias, fatigue, headache, impotence, and anemia. Minor increases in liver transaminases and alkaline phosphatase have been reported. Clofibrate, bezafibrate, and fenofibrate have been reported to potentiate the action of oral anticoagulants, in part by displacing them from their binding sites on albumin. Careful monitoring of the prothrombin time and reduction in dosage of the anticoagulant may be appropriate when treatment with a fibrate is begun.

A myopathy syndrome occasionally occurs in subjects taking clofibrate, gemfibrozil, or fenofibrate, and may occur in up to 5% of patients treated with a combination of gemfibrozil and higher doses of statins. To diminish the risk of myopathy, statin doses should be reduced when combination therapy of a statin plus a fibrate is employed. Several drug interactions may contribute to this adverse response. Gemfibrozil inhibits hepatic uptake of statins by OATP2. Gemfibrozil also competes for the same glucuronosyl transferases that metabolize most statins. As a consequence, levels of both drugs may be increased when they are coadministered. (Prueksaritanont et al., 2002b; Prueksaritanont et al., 2002c). Patients taking this combination should be instructed to be aware of the potential symptoms and should be followed at 3-month intervals with careful history and determination of CK values until a stable pattern is established. Patients taking fibrates with rosuvastatin should be followed especially closely even if low doses (5 to 10 mg) of rosuvastatin are employed until there is more experience with and knowledge of the safety of this specific combination. Fenofibrate is glucuronidated by enzymes that are not involved in statin glucuronidation. Thus, fenofibrate-statin combinations are less likely to cause myopathy than combination therapy with gemfibrozil and statins.

All of the fibrates increase the lithogenicity of bile. Clofibrate use has been associated with increased risk of gallstone formation; gemfibrozil and fenofibrate reportedly do not increase biliary tract disease.

Renal failure is a relative contraindication to the use of fibric acid agents, as is hepatic dysfunction. Combined statin-fibrate therapy should be avoided in patients with compromised renal function. Gemfibrozil should be used with caution and at a reduced dosage to treat the hyperlipidemia of renal failure. Fibrates should not be used by children or pregnant women.

Therapeutic Uses. Clofibrate is available for oral administration. The usual dose is 2 g per day in divided doses. This compound is little used but may be useful in patients who do not tolerate gemfibrozil or fenofibrate. Gemfibrozil (LOPID) is usually administered as a 600-mg dose taken twice a day, 30 minutes before the morning and evening meals. The TRICOR brand of fenofibrate is available in tablets or 48 and 145 mg. The usual daily dose is 145 mg. Generic fenofibrate (LOFIBRA) is available in capsules containing 67, 134, and 200 mg. TRICOR, 145 mg, and LOFIBRA, 200 mg, are equivalent doses.

Fibrates are the drugs of choice for treating hyperlipidemic subjects with type III hyperlipoproteinemia as well as subjects with severe hypertriglyceridemia (triglycerides >1000 mg/dl) who are at risk for pancreatitis. Fibrates appear to have an important role in subjects with high triglycerides and low HDL-C levels associated with the metabolic syndrome or type 2 diabetes mellitus (Robins, 2001). When fibrates are used in such patients, the LDL levels need to be monitored; if LDL levels rise, the addition of a low dose of a statin may be needed. Many experts now treat such patients first with a statin (Heart Protection Study Collaborative Group, 2003), and then add a fibrate, based on the reported benefit of gemfibrozil therapy (Rubins et al., 1999). However, statin-fibrate combination therapy has not been evaluated in outcome studies (American Diabetes Association, 2004). If this combination is used, there should be careful monitoring for myopathy

( i have choosen cecil because it is 2007 edtion so hopefully all new advances would have been added)

Imaging

Electrocardiography

Electrocardiographic findings, which are present in the majority of patients with acute PE, include ST segment abnormalities, T wave changes, and left or right axis deviation. Only one third of patients with massive or submassive emboli have manifestations of acute cor pulmonale, such as an S1-Q3-T3 pattern, right bundle branch block, P wave pulmonale, or right axis deviation. All of these findings are also nonspecific. Thus, the utility of electrocardiography in suspected acute PE arises more from its ability to establish or to exclude alternative diagnoses, such as acute myocardial infarction or pericarditis ( Chapter 77 ), rather than from diagnosis or exclusion of PE.

Chest Radiography

The chest radiograph is often abnormal in patients with acute PE, but it is nearly always nonspecific. Common findings include pleural effusion, atelectasis, pulmonary infiltrates, and mild elevation of a hemidiaphragm. Classic findings of pulmonary infarction, such as Hampton's hump and decreased vascularity (Westermark's sign), are suggestive of the diagnosis but are infrequent. PE should be considered in patients who have dyspnea and hypoxemia with a normal chest radiograph in the absence of bronchospasm or anatomic cardiac shunt. Under most circumstances, however, the chest radiograph cannot be used for conclusive diagnosis or exclusion. Although the radiograph may exclude other processes, such as pneumonia, pneumothorax, or rib fracture, which may cause similar symptoms, acute PE may frequently coexist with other underlying heart or lung diseases.

Spiral Computed Tomography

Spiral (helical) computed tomography (CT) can be used for diagnosis of both acute and chronic PE and has replaced ventilation-perfusion (VQ) scanning at many centers [/bThis technique involves continuous movement of the patient through the CT scanner and allows concurrent scanning by a constantly rotating gantry and detector system. Rapid scanning is performed with continuous acquisitions obtained during a single breath. Retrospective reconstructions can be performed. An intravenous injection of contrast material is required for imaging of the pulmonary vasculature

Increased experience and advances in multislice scanning provide rapid images with a sensitivity in the 80 to 90% range and specificity to consistently above 90%. By also including images of the legs without additional contrast material, the sensitivity for VTE was increased from about 83% to about 90% in one large study, in which the specificity was 95%. The imperfect results should not be surprising because even the â€œgold standardâ€ test, pulmonary arteriography, is not perfect for smaller, peripheral emboli. Spiral CT is most sensitive for detecting emboli in the main, lobar, or segmental pulmonary arteries; its specificity for clot in these vessels is also excellent. For subsegmental emboli, spiral CT appears to be less accurate, but the importance of emboli of this size has been questioned. An advantage of spiral CT over VQ scanning and arteriography is the ability of CT to define nonvascular conditions such as lymphadenopathy, lung tumors, emphysema, and other parenchymal abnormalities as well as pleural and pericardial disease. A second advantage of spiral CT over other diagnostic methods is the rapidity with which the scan can be performed. Conversely, disadvantages of CT include its poor sensitivity for detecting clots in small vessels, the fact that it is not portable at present, and the fact that patients with significant renal insufficiency cannot be scanned without risk of renal failure.

Data suggest that the outcome after a normal spiral CT scan is excellent, with the risk of recurrence (development of acute VTE) being exceedingly low. For example, a strategy using a dichotomized version of the Wells score (see Table 99-3 ), D-dimer testing, and CT imaging can reduce the need for expensive testing and provide good outcomes at 3 months

Increased experience and advances in multislice scanning provide rapid images with a sensitivity in the 80 to 90% range and specificity to consistently above 90%. By also including images of the legs without additional contrast material, the sensitivity for VTE was increased from about 83% to about 90% in one large study, in which the specificity was 95%. The imperfect results should not be surprising because even the â€œgold standardâ€ test, pulmonary arteriography, is not perfect for smaller, peripheral emboli. Spiral CT is most sensitive for detecting emboli in the main, lobar, or segmental pulmonary arteries; its specificity for clot in these vessels is also excellent. For subsegmental emboli, spiral CT appears to be less accurate, but the importance of emboli of this size has been questioned. An advantage of spiral CT over VQ scanning and arteriography is the ability of CT to define nonvascular conditions such as lymphadenopathy, lung tumors, emphysema, and other parenchymal abnormalities as well as pleural and pericardial disease. A second advantage of spiral CT over other diagnostic methods is the rapidity with which the scan can be performed. Conversely, disadvantages of CT include its poor sensitivity for detecting clots in small vessels, the fact that it is not portable at present, and the fact that patients with significant renal insufficiency cannot be scanned without risk of renal failure.

Data suggest that the outcome after a normal spiral CT scan is excellent, with the risk of recurrence (development of acute VTE) being exceedingly low. For example, a strategy using a dichotomized version of the Wells score (see Table 99-3 ), D-dimer testing, and CT imaging can reduce the need for expensive testing and provide good outcomes at 3 months

Ventilation-Perfusion Scanning

A normal perfusion scan ( Fig. 99-3 ) excludes PE with a high enough degree of certainty that further diagnostic evaluation is almost never necessary. Although large, central, nonocclusive emboli might transiently permit tracer to perfuse the lungs normally, this phenomenon is exceedingly unusual, and PE should be pursued only when the clinical suspicion is exceptionally high. Matching areas of decreased ventilation and perfusion in the presence of a normal chest radiograph generally represent a process other than PE. However, low- or intermediate-probability (nondiagnostic) VQ scans are commonly found with PE, and further evaluation with pulmonary arteriography or leg studies is often appropriate in such situations
The specificity of high-probability scans is 97%, but the sensitivity is only 41%. When the clinical suspicion of PE is considered very high, PE is present in 96% of patients with high-probability VQ scans, 66% of patients with intermediate scans, and 40% of patients with lowprobability scans. Thus, the diagnosis of PE should be rigorously pursued even when the lung scan is of low or intermediate probability if the clinical setting strongly suggests the diagnosis. Although the VQ scan either may be diagnostic of PE in higher risk patients or may exclude the possibility with sufficient certainty in low-risk patients, it is often nondiagnostic. Even in the latter circumstance, however, it may serve as a guide for the interventional radiologist by directing selective dye injection to minimize the contrast load and to limit the duration of pulmonary arteriography.

Pulmonary Arteriography

Pulmonary arteriography, which remains the gold standard for the diagnosis of acute PE, is an extremely sensitive and specific test. Major nonfatal complications occur with 1% of angiograms, and death occurs in 0.5%. Its clinical role has been for patients in whom PE must be diagnosed or excluded, but preliminary testing has been nondiagnostic. However, with the advent of CT, pulmonary angiography is now used infrequently.
Magnetic Resonance Imaging

Magnetic resonance imaging can be used in suspected PE, but the main advantage of magnetic resonance imaging at present is its excellent sensitivity and specificity for the diagnosis of DVT ( Chapter 81 ). Disadvantages include the potential difficulty in transporting and studying more critically ill patients.

Echocardiography

Echocardiography ( Chapter 53 ), which can often be obtained more rapidly than either lung scanning or pulmonary arteriography, may reveal abnormalities of right ventricular size or function that strongly support the diagnosis of hemodynamically significant PE. However, because these patients often have underlying cardiopulmonary disease such as chronic obstructive lung disease, neither right ventricular dilation nor hypokinesis can be reliably used even as indirect evidence of PE. In the setting of documented PE, echocardiographic evidence of right ventricular dysfunction can identify patients who may benefit from thrombolytic therapy (see Treatment).

so best or gold standard is still pulmonary angiography.but mosat used is ct.

so if they mean best by gold standard answer is pulmonary angiography but the answer will depend on examiner.

if they have asked next best answer will be ct and if best answer will be angio so my peak of best is pulmonary angiography but still i would suggest the persons who are counting score inrespective of answer should take this as negative.because answer dpend upon examiner 's wish,and his experience.

With respect to localized amyloidosis, cardiac
amyloidosis of the wild type or nonvariant TTR type is common
after 80 years of age;
there was some confusion due to Harrison table but above line I think will clear the doubts that after 80 years(senile) ttr type is common

Background: Agenesis of the corpus callosum (ACC) is an anomaly that may occur in isolation or in association with other CNS or systemic malformations. Because the corpus callosum may be partially or completely absent, the term dysgenesis has also been used to describe the spectrum of callosal anomalies.

Pathophysiology: Dysgenesis of corpus callosum is usually a sporadic occurrence, although the incidence is increased in patients with trisomy 18, trisomy 13, and trisomy 8. Several familial cases have been reported. Organ systems other than the CNS, particularly the musculoskeletal and genitourinary systems, may be affected as well.

Fibers of the corpus callosum arise from the superficial layers of the cerebral cortex and they project to the homotypic region of the contralateral cortex by passing through the corpus callosum while crossing the midline. Disturbance of embryogenesis in the first trimester of gestation by some unknown insult leads to failure of the callosal axons to pass across the midline. These arrested axons form the longitudinally oriented bundles of Probst that are located medial to the lateral ventricles in patients with agenesis.

Spectrum of abnormalities

ACC can be complete, partial, or atypical.

With complete agenesis, the corpus callosum is totally absent.

With partial agenesis (hypoplasia), the anterior portion (posterior genu and anterior body) is formed, but the posterior portion (posterior body and splenium) is not formed. The rostrum and the anterior/inferior genu are also not formed.

An atypical appearance occurs when the anterior to posterior formation is not respected.

In holoprosencephaly, callosal anomalies are atypical, eg, the splenium may be present without a genu or body. In middle interhemispheric fusion, a variety of holoprosencephaly, the genu and splenium may be present without the callosal body.

With pseudo corpus callosum, in conditions of complete or partial agenesis, the hippocampal commissure may become enlarged and appear like the posterior part of the corpus callosum.

Secondary destruction of corpus callosum occurs when the genu and anterior body are destroyed, leaving the posterior portion of the corpus callosum intact. This can occur secondary to porencephaly or schizencephaly, in transcallosal surgical approaches to the lateral and third ventricle, and with hemisection of the callosum for the treatment of seizures.

Other cerebral malformations may coexist with callosal dysgenesis. Examples of these include interhemispheric cysts; intracranial lipomas; and disorders of neuronal migration, such as schizencephaly, neuronal heterotopias, lissencephaly, and pachygyria.

Frequency of abnormalities

The frequencies of some of the more commonly associated anomalies are as follows:

CNS anomalies (85%)

Dandy Walker cyst (11%)

Interhemispheric cysts

Hydrocephalus (30%)

Midline lipoma of corpus callosum (10%)

Arnold-Chiari malformation (7%)

Midline encephalocele

Porencephaly

Holoprosencephaly

Hypertelorism median cleft syndrome

Polymicrogyria

Gray-matter heterotopia

Cardiovascular, GI, and GU anomalies (62%)

Frequency:

In the US: The reported frequency is 0.7-5.3%.
Internationally: The frequency is not known but could be similar to that in the US.
Mortality/Morbidity:

ACC may occur as an isolated defect, but it is frequently associated with other malformations, chromosomal abnormalities, and genetic syndromes.
Although ACC has been found in asymptomatic individuals, it is generally considered a potential marker for neurologic impairment.
In children, the prognosis is frequently related to other associated abnormalities.
Sex: ACC is reported to be more common in males than in females.

Age: ACC is a congenital or a developmental anomaly, and therefore, is present at the time of birth. In many cases, agenesis is diagnosed later in infancy or in childhood because of its associated congenital malformations.

Anatomy :

Development and Anatomy

The corpus callosum develops from the lamina reuniens in the telencephalon, and it begins to appear between the anterior and hippocampal commissures at about 10.5 weeks. The adult form of the corpus callosum is achieved by 17 weeks' gestational age. Initial formation of the corpus callosum occurs in the genu and the body, progressing posteriorly. The anterior genu and rostrum develops last, folding back under the genu. The callosum thickens with increasing myelination.

When the corpus callosum is absent, the third ventricle is often high riding, extending superiorly between the lateral ventricles. On coronal imaging, a candelabra appearance occurs, with the third ventricle forming the central vertical portion and the lateral ventricles the peripheral arms of the candelabra. On axial imaging, the lateral ventricles are parallel.

Medial to the lateral ventricles, longitudinal bundles of white matter are present. These are known as Probst bundles and presumably would have formed a normal corpus callosum. Probst bundles are seen best on coronal or axial T1-weighted MRIs. The occipital horns of the lateral ventricles are dilated in patients with ACC, probably because of a deficiency of peritrigonal white matter fibers. This anatomic finding is known as colpocephaly. When the corpus callosum is absent, the cingulate gyrus is inverted, the normal cingulate sulcus is absent, and the medial cerebral sulci radiate toward the midline in a radial configuration. This finding is especially helpful in evaluating newborns in whom the corpus callosum is normally thin.

The hippocampal formations are frequently hypoplastic in patients with ACC, with resulting mild dilatation of the temporal horns. In partial callosal agenesis, the posterior body, splenium and rostrum are usually absent. Absence of the posterior body and splenium is especially common in patients with a Chiari II malformation. Barkovich has described the unusual absence of the genu or the midbody of the corpus callosum in patients with atypical or mild forms of holoprosencephaly.

Associated midline cysts are noted in some cases. The exact origin and nature of these cysts is controversial. While some of these cysts represent a dilated superiorly migrated third ventricle, others represent true midline cysts that may be lined by ependymal cells or by arachnoid membranes.

Types of midline cyst formation

Raybaud and Girard suggest that there are 3 types of midline cyst formation in association with agenesis or hypogenesis of the corpus callosum.

Type 1 is a large midline cyst that communicates with third ventricle and the lateral ventricles.

Type 3 involves complex, multilocular cysts that are asymmetric and independent of the ventricles. Cortical malformations are uncommon. With large cysts, the ipsilateral lateral ventricle may be compressed, and the contralateral ventricle may be obstructed and enlarged (hydrocephalus). A CT cystogram may be helpful in identifying the communications between the loculations of the cysts and with the ventricles and in guiding the placement of a ventriculostomy shunt.

Associated anatomic abnormalities

Other anatomic abnormalities in patients with ACC include hydrocephalus; cephaloceles; and neuronal migration disorders such as lissencephaly, schizencephaly, gray matter heterotopias, pachygria, and polymicrogyria.

Clinical Details: The white matter fibers forming the corpus callosum predominantly connect symmetrical regions in the frontal, parietal, temporal, and occipital lobes. Experimental observations indicate that the corpus callosum allows the sharing of learning and memory between the two cerebral hemispheres.

The clinical manifestations of callosal agenesis can be described under 2 headings: nonsyndromic and syndromic.

Nonsyndromic forms are the most common. An unknown, though probably small, proportion of patients are completely asymptomatic, or more commonly, their condition is incidentally discovered during neuroimaging. Patients may present with mental retardation or delayed development, seizures, and cerebral palsy. Macrocephaly may be seen due to hydrocephalus sometimes associated with interhemispheric cysts.

A number of syndromes may be associated with ACC. Some of the more common ones include Dandy-Walker syndrome, Aicardi syndrome, fetal alcohol syndrome, and several of the trisomies.

Preferred Examination: The diagnosis of callosal agenesis depends on neuroimaging. In the newborn prior to closure of the anterior fontanelle, screening ultrasonography (US) can clearly show the absence of the corpus callosum, parallel lateral ventricles, interhemispheric cysts, hydrocephalus, and other related anomalies. US was the first imaging modality to allow direct sagittal imaging of callosal dysgenesis.

Antenatal diagnosis of ACC is possible from about 20 weeks' gestation. Characteristic intrauterine US findings include colpocephaly and parallel ventricular walls. CT findings are also diagnostic of ACC. Parallel lateral ventricles, colpocephaly, and extension of the third ventricle into the interhemispheric fissure are particularly pertinent findings. In patients with ACC and an interhemispheric cyst, the preoperative injection of nonionic water-soluble contrast material into the cystic loculations for CT enables assessment of the ventricular system or of the communication of the cystic components with one another.

MRI is currently the imaging procedure of choice in infants and children with ACC, even in patients who have previously undergone CT and US examinations. The multiplanar capability and high soft-tissue contrast possible with MRI permits confident diagnosis of ACC and its associated anomalies, especially neuronal migration anomalies or atypical forms of holoprosencephaly. These entities may be extremely subtle or indiscernible on CT or US images.

Limitations of Techniques: Both CT and US can depict ACC, but MRI is the preferred imaging modality because of its greater sensitivity for depicting associated cerebral anomalies.

Findings: Axial CT shows parallel ventricles and continuation of the interhemispheric fissure with the third ventricle in patients with ACC. Colpocephaly can easily be visualized.

Nonenhanced axial CT can show an interhemispheric cyst. In complex types of multilocular interhemispheric cysts associated with callosal agenesis, a CT cystogram or ventriculogram can be obtained after iohexol is introduced into the cyst to establish which of the CSF collections communicate with each other or with the ventricular system.

Degree of Confidence: Although CT findings can suggest the diagnosis, MRI and US show the anatomic findings of ACC better than CT. MRI is the preferred imaging modality, especially for the diagnosis of partial agenesis and for the depiction of associated anomalies. MRI Section 6 of 9
Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Pictures Bibliography

Findings: The MRI findings in ACC are clearly demonstrated on the sagittal projection. Sagittal T1-weighted images clearly demonstrate the exact extent of callosal dysgenesis. In complete agenesis, the corpus callosum is not visualized, whereas in a hypogenetic corpus callosum, the later forming structures are usually absent. Therefore, the corpus callosum may show a posterior genu; a posterior genu and anterior body; a genu and an entire body; or an entire genu, body, and splenium with the exception of the rostrum. The third ventricle may be high riding and interposed between the bodies of the lateral ventricles.

Loss of the supporting function of the corpus callosum results in upward bulging of the roof of the third ventricle into the interhemispheric fissure. This upward herniation of the distended third ventricle is generally referred to as the interhemispheric cyst, but it should not be confused with a true dorsal or arachnoid cysts of the interhemispheric fissure found in some cases of callosal agenesis. The herniated third ventricle or true cyst may be located in the midline, separating the cerebral hemispheres, or it may be located predominantly to one side of the falx or the other. The herniated third ventricle is of variable size, sometimes extending superiorly all the way to the inner table of the calvaria.

An arachnoid or dorsal cyst generally does not communicate with the third or lateral ventricles, and it may be multiseptated. Hemorrhage may occur within the cysts, markedly changing their signal intensity on MRIs.

Coronal and axial MRI sections are best for demonstrating the longitudinal callosal bundles of Probst. They represent nondecussated callosal fibers. Instead of crossing in the midline, these fibers deviate at the interhemispheric fissure to run along the medial borders of the lateral ventricles from the frontal paraolfactory cortex to the occipital region. Their volume is less than that of the fibers in the normal corpus callosum, and their size varies.

The anterior commissure is usually present and occasionally larger or smaller than normal. It is best seen on sagittal or axial T1-weighted images. The hippocampal commissure is usually absent or hypoplastic but sometimes may be enlarged. The lateral ventricles may have a colpocephalic appearance with a localized dilatation of the atria and occipital horns. The lateral ventricles are impressed upon superomedially by the adjacent bundles, which are more marked in the frontal regions where the bundles are thickest. They also appear widely separated and medially concave, with the upper corners turned up and pointed. This finding is called [bleep]'s horns or the bat-wing conformation. The foramen of Monro may be enlarged. The cingulate gyri are not rotated and the cingulate sulcus is absent with the resultant radial pattern of sulci in the medial surface of the cerebral hemisphere. This finding is helpful in evaluating the newborns in whom the corpus callosum is normally thin.

Keyhole dilatation of the temporal horns, secondary to incomplete inversion of the hippocampal formation, is often present. This finding indicates the intimate relationship between the development of the corpus callosum and the limbic system. A large percentage of patients with dysgenesis of the corpus callosum have a large interhemispheric cyst, which may or may not communicate with the ventricular system.

The cyst is frequently associated with hydrocephalus. The exact origin of the cyst is not known. Some suggest that it is a dilated third ventricle or a true arachnoid cyst. At autopsy, the lining of the cyst may contain ependymal or arachnoid cells. On MRIs, the cyst may have a high protein content, in which case, the signal intensity on the T1-weighted image is greater than that of CSF.

A pericallosal lipoma of the corpus callosum is seen as a high-signal-intensity mass on T1 weighted images usually dorsal to the corpus callosum, which may be associated with callosal dysgenesis.

The differential diagnosis of this condition is very limited owing to the characteristic imaging appearance. For example, in certain cases of hydrocephalus in infants it may be difficult sometimes to visualize a corpus callosum that is very thin. But on careful observation of the sagittal images on MR, the radial convergence of sulci that is seen with ACC is not seen and a thin corpus can usually be identified. The midline interhemispheric cysts may be confused with midline arachnoid cyst (suprasellar, collicular) or with prominent cavum septum pellucidum and cavum vergae.

Degree of Confidence: With the exception of US in the sagittal projection, MRI is best for directly visualizing the anatomic appearance of the corpus callosum. The neuropathologic abnormalities intrinsic to callosal dysgenesis, as well as the associated brain anomalies, are portrayed in exquisite detail on sagittal, axial, and coronal MRIs. Only MRI can be used to reliably detect subtle partial callosal dysgenesis.

Enneking and others have demonstrated the desirability of staging both benign and malignant musculoskeletal tumors to aid in treatment decision making and to allow meaningful comparisons of treatment methods. Both benign and malignant tumors of bone and soft tissue can be staged according to the Enneking staging system ( Table 19-1 ). The stages of benign tumors are designated by Arabic numbers and malignant tumors are designated by Roman numerals.
Benign tumors are staged as follows: stage 1, latent; stage 2, active; and stage 3, aggressive. Stage 1 lesions are intracapsular, usually asymptomatic, and frequently incidental findings. Roentgenographic features include a well-defined margin with a thick rim of reactive bone. There is no cortical destruction or expansion. These lesions do not require treatment because they do not compromise the strength of the bone and usually resolve spontaneously. An example is a small asymptomatic nonossifying fibroma discovered incidentally on roentgenograms taken to evaluate an unrelated injury. Stage 2 lesions also are intracapsular but are actively growing and therefore can cause symptoms or lead to pathological fracture. They have well-defined margins on roentgenograms but may expand and thin the cortex. Usually they have only a very thin rim of reactive bone. Treatment usually consists of extended curettage. Stage 3 lesions are extracapsular. Their aggressive nature is apparent both clinically and roentgenographically. They usually have broken through the reactive bone and possibly the cortex. MRI may demonstrate a soft tissue mass, and metastases may be present in up to 5% of patients with these lesions. Treatment consists of extended curettage and marginal or even wide resection, and local recurrences are common.
Musculoskeletal sarcomas also can be staged according to the surgical staging system as described by Enneking et al. This system was designed to incorporate the most significant prognostic factors into a system of progressive stages that helps to guide surgical and adjuvant treatments. The system is based on the histological grade of the tumor, its local extent, and the presence or absence of metastases. Low-grade lesions are designated as stage I. These lesions are well-differentiated, have few mitoses, and exhibit only moderate cytological atypia. The risk for metastases is low (<25%). High-grade lesions are designated as stage II. They are poorly differentiated with a high mitotic rate and a high cell/matrix ratio. Stages I and II lesions are subdivided according to the extent of local growth. Stages IA and IIA lesions are contained within well-defined anatomical compartments. Anatomical compartments are determined by the natural anatomical barriers to tumor growth such as cortical bone, articular cartilage, fascial septa, or joint capsules. Stages IB and IIB lesions extend beyond the compartment of origin. Stage III refers to any lesion that has metastasized regardless of the size or grade of the primary tumor. No distinction is made between lymph node metastases or distant metastases because both circumstances are associated with an equally poor prognosis.

Most common site of subependymal giant cell astrocytomas is:
a. Foramen of Monro
b. Temporal horn of the lateral ventricle
c. Trigone of the lateral ventricle
d. Fourth ventricle

answer a.foramen of monro

refrence oxford text book of oncology

Tuberous sclerosis is characterized by facial angiofibroma, together with visceral and central nervous system lesions (most often cortical nodules; tubers). Giant cell astrocytoma is the central nervous system tumour classically associated with tuberous sclerosis. It is usually benign, and most commonly occurs at the foramen of Monro arising in the subependymal foci of giant astrocytes seen in this syndrome.(15) Von Hippelâ€“Lindau syndrome consists of haemangioblastomas within the central nervous system together with retinal angiomatosis. It is also associated with renal carcinoma and in some cases with phaeochromocytoma.(16) Brain tumours have been described in patients with familial adenomatous polyposis, and this association is named Turcot's syndrome. The majority are gliomas or medulloblastomas and usually present before the diagnosis of familial adenomatous polyposis.(17),(18) Medulloblastomas are also found in approximately 5 per cent of cases of Gorlin's syndrome.(19)

18 year old male presents with pectus excavatum. He denies history of any dyspnoea or chest pain. On examination there is mild pectus excavatum and intermittent wheezing on exertion. Surgery in this patient is indicated if he has:
a. FEV1 / FVC less than 0.60
b. Limiation of maximum inspiration during exercise
c. Peak work capacity 60% of expected
d. Functional work capacity 80% of expected

answer c.peak work capacity 60% of expected

nelson 17th edition page 1467 chapter 409.1

Pectus Excavatum (Funnel Chest)
Pathogenesis.
Midline narrowing of the thoracic cavity is usually an isolated skeletal abnormality. The cause is unknown. It may be associated with a connective tissue disorder (i.e., Marfan syndrome) or rickets, or it may be acquired.

Clinical Manifestations.

The deformity is present at or shortly after birth but is usually not associated with any symptoms at that time. Over time, decreased exercise tolerance, chest pain, palpitations, recurrent respiratory infections, wheezing, stridor, and cough may be present. Because of the cosmetic nature of this deformity, many children experience significant psychological stress. Physical examination may reveal a narrowed anteroposterior diameter, rounded shoulders, kyphoscoliosis, protuberant abdomen, left shift of the cardiac impulse, and an innocent systolic murmur.

Diagnosis.

Lateral chest radiograms demonstrate the depression. An electrocardiogram may show a right-axis deviation. Mitral valve prolapse, Wolff-Parkinson-White syndrome, bronchial atresia, and bronchomalacia are associated. Results of pulmonary function tests may be normal or may show a restrictive defect, if the pectus deformity is severe. Exercise testing may demonstrate either normal tolerance or limitations from underlying limited habitual activity or cardiopulmonary dysfunction. Lowered ventilatory reserves at peak exercise are common, although the clinical significance of these findings remains unclear.

Treatment.
Corrective surgery is beneficial for individuals with restrictive lung disease. Although surgery itself does not reverse the lung restriction, it may halt the progression of cardiopulmonary compromise. For teenagers with exercise limitations, surgical repair may result in improved exercise tolerance. Normalization of lung perfusion scans and maximal voluntary ventilation have also been seen after surgery. Surgery is often performed for psychological or cosmetic reasons.

now ou can see that they have given exercise intolrence that means peak exercise capacity and not functional.

they have restrictive lung disease so a. is ruled out.

now las two lines creates some confuion regarding b but maxiumum inspiration does not mean voluntary(during exrcise we do not voluntary increase our ventialtion) and other thing is that it is stated no improvement in lung function is seen after surgery.

i have looked into thoracic surgery,pediatric surgery books but could not find better refrence than this.

A 30 year old male patient presents with a peptic ulcer in the posterior duodenum with a bleeding vessel at the base. The bleeding is not controlled endoscopically. On examination his heart rate is 100/min, BP is 110/76 mm of Hg and Hb is 10 gm/dl after transfusion. Next step in his management will be:
a. Proton pump inhibitors
b. Duodenotomy with controlled bleeder and pyloroplasty
c. Duodenotomy with controlled bleeder and truncal vagotomy with antrectomy
d. Partial gastrectomy involving the bleeding ulcer

refrence schwart 8the edition chapter 25 table 25-12

answer c.duodenotomy with controlled bleeder and truncal vagotomy with antrectomy

Table 25-12 Surgical Options in the Treatment of Duodenal and Gastric Ulcer Disease

Indication Duodenal Gastric
Bleeding 1. Oversewa

2. Oversew, V+D

3. V+A

1. Oversew and biopsya

2. Oversew, biopsy, V+D

3. Distal gastrectomyb

Perforation 1. Patcha

2. Patch, HSVb

3. Patch, V+D

1. Biopsy and patcha

2. Wedge excision, V+D

3. Distal gastrectomyb

Obstruction 1. HSV + GJ

2. V+A

1. Biopsy; HSV + GJ

2. Distal gastrectomyb

Intractability/nonhealing 1. HSVb

2. V+D

3. V+A

1. HSV and wedge excision

2. Distal gastrectomy

aUnless the patient is in shock or moribund, a definitive procedure should be considered.

Indications for operation for bleeding duodenal ulcers are massive hemorrhage that is unresponsive to endoscopic control, and transfusion requirement of more than 4 to 6 units of blood, despite attempts at endoscopic control. Lack of availability of a therapeutic endoscopist, recurrent hemorrhage after one or more attempts at endoscopic control, lack of availability of blood for transfusion, repeat hospitalization for bleeding duodenal ulcer, and concurrent indications for surgery such as perforation or obstruction, also are indications for surgery. The mortality rate for surgery for bleeding duodenal ulcer is 10 to 20%. Early operation should be considered in patients over 60 years of age, those presenting in shock, those requiring more than 4 units of blood in 24 hours or 8 units of blood in 48 hours, those with rebleeding, and those with ulcers greater than 2 cm in diameter or strategically located as described above.

The two operations most commonly used for bleeding duodenal ulcer are V+D combined with oversewing of the ulcer, or V+A. The trade-off appears to be an increased risk of rebleeding with V+D, compared to the increased operative mortality of V+A. When the mortality for reoperation for rebleeding is considered, the overall mortality is probably comparable for the two approaches. Patients who are in shock or medically unstable should not have gastric resection.

An initial pyloromyotomy incision allows access to the bleeding posterior duodenal ulcer, and an expeditious Kocher maneuver allows the surgeon to control the hemorrhage with the left hand if necessary. Heavy suture material on a stout needle is used to place figure-of-eight sutures or a U-stitch in order to secure the bleeding vessel at the base of the posterior duodenal ulcer. Multiple sutures are usually necessary. Once the surgeon is unequivocally convinced that hemostasis is secure, a pyloroplasty can be performed. A truncal vagotomy completes the operation. If V+A is selected, smaller ulcers are resected with the specimen, but larger bleeding duodenal ulcers must often be left behind in the duodenal stump. If this is the case, suture hemostasis must be attained and a secure duodenal closure accomplished. The anterior wall of the open duodenum can be sutured to either the proximal or distal lip of the posterior ulcer once the bleeding vessel has been sutured. The duodenal closure can be buttressed with omentum and the duodenum should be decompressed, either with a lateral duodenostomy or retrograde duodenostomy tube via the proximal jejunum. Use of a feeding jejunostomy is also considered. A Billroth II anastomosis is preferred because it avoids the extensive mobilization necessary for Billroth I, and because it keeps the ulcer out of the acid stream if it is left behind.

What is true about linkage analysis in familial gene disorders:
a. Characteristic DNA polymorphism in a family is associated with disorders
b. Characteristic DNA polymorphism WITH A CLINICAL PHENOTYPE
C.Useful to make pedigree chart to show affected and non-affected family members
D.Used to make a pedigree chart to show non-paternity

answer: a.

Characteristic DNA polymorphism in a family is associated with disorders

harrison page 372-373

GENETIC LINKAGE
Genetic linkage refers to the fact
that genes are physically connected, or linked, to one
another along the chromosomes. Two fundamental
principles are essential for understanding the concept
of linkage: (1) when two genes are close together
on a chromosome, they are usually transmitted
together, unless a recombination event separates
them (Fig. 56-4); and (2) the odds of a crossover, or recombination
event, between two linked genes is proportional to the distance that
separates them. Thus, genes that are further apart are more likely to
undergo a recombination event than genes that are very close together.
The detection of chromosomal loci that segregate with a disease by
linkage can be used to identify the gene responsible for the disease
(positional cloning) and to predict the odds of disease gene transmission
in genetic counseling.
Polymorphisms are essential for linkage studies because they provide
a means to distinguish the maternal and paternal chromosomes
in an individual. On average, 1 out of every 1000 bp varies from one
person to the next. Although this degree of variation seems low (99.9%
identical), it means that3 million sequence differences exist between
any two unrelated individuals and the probability that the sequence at
such loci will differ on the two homologous chromosomes is high
(often 70 to 90%). These sequence variations include VNTRs, short
tandem repeats (STRs), and SNPs. Most STRs, also called polymorphic
microsatellite markers, consist of di-, tri-, or tetranucleotide repeats
that can be measured readily using PCR (Fig. 56-10).

Characterization of SNPs, using DNA chips, provides a promising means for
rapid analysis of genetic variation and linkage. Although this sequence
variation usually has no apparent functional consequence, it provides
much of the basis for variation in genetic traits.
In order to identify a chromosomal locus that segregates with a
disease, it is necessary to determine the genotype or haplotype of DNA
samples from one or several pedigrees. One can then assess whether
certain marker alleles cosegregate with the disease. Markers that are
closest to the disease gene are less likely to undergo recombination
events and therefore receive a higher linkage score. Linkage is expressed
as a lod (logarithm of odds) score—the ratio of the probability
that the disease and marker loci are linked rather than unlinked. Lod
scores of 3 (1000:1) are generally accepted as supporting linkage,
whereas a score of 2 is consistent with the absence of linkage.

An example of the use of linkage analysis is shown in Fig. 56-10.
In this case, the gene for the autosomal dominant disorder, MEN-1, is
known to be located on chromosome 11q13. Using positional cloning,
the MEN1 gene was identified and shown to encode menin, a tumor
suppressor. Affected individuals inherit a mutant form of the MEN1
gene, predisposing them to certain types of tumors (parathyroid, pituitary,
pancreatic islet) (Chap. 330). In the tissues that develop a tumor,
a “second hit” occurs in the normal copy of the MEN1 gene. This
somatic mutation may be a point mutation, a microdeletion, or loss of
a chromosomal fragment (detected as loss of heterozygosity, LOH).
Within a given family, linkage to the MEN1 gene locus can be assessed
without necessarily knowing the specific mutation in the MEN1 gene.
Using polymorphic STRs that are close to the MEN1 gene, one can
assess transmission of the different MEN1 alleles and compare this
pattern to development of the disorder to determine which allele is
associated with risk of MEN-1. In the pedigree shown, the affected
grandfather in generation I carries alleles 3 and 4 on the chromosome
with the mutated MEN1 gene and alleles 2 and 2 on his other chromosome
11. Consistent with linkage of the 3/4 genotype to the MEN1
locus, his son in generation II is affected, whereas his daughter (who
inherits the 2/2 genotype from her father) is unaffected. In the third
generation, transmission of the 3/4 genotype indicates risk of developing
MEN-1, assuming that no genetic recombination between the
3/4 alleles and the MEN1 gene has occurred. After a specific mutation
in the MEN1 gene is identified within a family, it is possible to track
transmission of the mutation itself, thereby eliminating uncertainty

This is a case of cervical incompetence causing recurrent 2nd trimester abortion
-Classically it is assoc with painless cervical dilatation in 2nd trimester with prolapse and balloning of membranes into the vagina followed by expulsion of an immature fetus.
-Diagnosis by,
a.premenstrual hysterocervicogaphy shows "funnel shaped shadow".
b.TVUS findings-cervical length <3cm,"FUNNELLING-ballooning of membranes into a dilated internal os but a closed external os",width of int. os >1.5cm in T1.
Management;
-during preg.-rest,reassurance,TLC[tender loving care!],US monitoring of a viable fetus
-treatment of underlying etiologies- natural micronised progesterone for LPD[lutal phase defect],low dose aspirin or aspirin+heparin for assoc. antiPL-antibody syn,......
-CIRCLAGE OPERATION-The tratment of classical cervical incompetence is cerclage.
The operation is performed to surgically reiforce the weak cervix by some type of purse string suturing.
bleeding,ruptured membranes and uterine contractions are C/I ti cerclage.
US to confirm a living fetus and to exclude fetal anomalies should precede cerclage.also cervical specimens to r/o chlammydia or gonorrhoeal infections is sent for examination.
cerclage is performed prophylactically b/w 12-16 wks or emergently following cervical dilatation.
Two types of cerclage poerations are performed-MCDONALD'S operation[simple procedure] and SHIRODKAR'S operation[complicated.].both have a success rate of 85-90%,but most practitioners reserve the modified Shirodkar's procedure for women with a previous failure of MCDONALD'S cerclage or those with structural cervical abnormalities.
so ans------->C.

hey that lady presented with abdominal pain for sure.that means she is going to abort anyway & u can not give a stitch

answer should be dinoprost because there r no chances u can prevent abortion.actually if stitch is given previously,u have to remove it as pain in abdomen starts otherwise cervical tearing occurs(it is called bucket handle tear).& how can u give a stitch to a pt already presenting with pain?
& option B was not progesterone but misoprostol

No where I could find seprate complications of emergency tracheostomy complications are mentioned together
And the other thing is in midline tracheostomy(which is also done as a part of emmegency tracheostomy) isthmus is normally devided and ligated.so I think it is not the complication

Vascular Injury
The following alerts you to several vessels that may bleed during tracheostomy.279
The anterior jugular veins may be encountered as the investing fascia is incised.
The venous thyroid plexus over the thyroid gland drains into the thyroid veins. The inferior thyroid veins drain inferiorly into the brachiocephalic veins, either forming a single stem or draining separately. The inferior thyroid vein is often asymmetric, hence, more liable to injury.
The branches of the superior and inferior thyroid arteries may anastomose across the midline.
A thyroid ima artery is very occasionally present, and must be ligated if found.
The brachiocephalic artery and left brachiocephalic vein can be injured if sharp dissection is carried too far downward. The artery can be eroded by a tracheostomy tube, resulting in a tracheoarterial fistula.
The subclavian artery and vein can be compromised by a tracheostomy tube that is incorrectly curved or placed too low (Fig. 1-90).
The common carotid artery can be injured when attempting a tracheostomy in the newborn. Moreover, it has been mistaken for the trachea. The left common carotid artery may arise from the brachiocephalic trunk, thereafter crossing the lower part of the cervical tracheaOrgan Injury
Esophagus
Injury to the esophagus usually occurs not from errors of perception of the Anatomy
, but from errors in the use of the tracheostomy tube. It is possible, however, to create an iatrogenic tracheoesophageal fistula by careless manipulation.280
Pneumothorax and Pneumomediastinum
Pneumothorax and pneumomediastinum also have been reported.
Recurrent Laryngeal Nerves
Injury to these nerves can occur during tracheostomy as well as during thyroidectomy (see "Anatomic Complications of Thyroidectomy").
Larynx
Too high a tracheostomy can result in direct injury to the vocal cords. Placement of the tube through the thyrohyoid membrane can also produce vocal cord injury.279 The stoma should be formed below the first ring.
Posttracheostomy Swallowing Dysfunction
The adverse effect of a cuffed tracheostomy tube on the swallowing mechanism was studied by Bonanno.281 Evaluation of the maxillary, glossopharyngeal, recurrent, and external laryngeal nerves revealed that nerve injury was not a factor. Bonanno concluded that the dysfunction was produced by inhibition of elevation and anterior rotation of the larynx and by failure of the hypopharyngeal sphincter to open completely

I would like to correct . Answer for this is Inferior thyroid artery. It enters from lower poles of the thyroid. Isthmus is definitely injured.
I have checked it in anat book and also got mail from AIIMS lecturer. He gave reference of cummings textbook.

thanks .yes it looks like inferior thyroid artery is the answer i am posting exat lines from moore clinical Anatomy 5th edition Tracheostomy
A transverse incision through the skin of the neck and anterior wall of the trachea (tracheostomy) establishes an airway in patients with upper airway obstruction or respiratory failure (Fig. B8.12). The infrahyoid muscles are retracted laterally, and the isthmus of the thyroid gland is either divided or retracted superiorly. An opening is made in the trachea between the first and second tracheal rings or through the second through fourth rings. A tracheostomy tube is then inserted into the trachea and secured. To avoid complications during a tracheostomy, the following anatomical relationships are important:
The inferior thyroid veins arise from a venous plexus on the thyroid gland and descend anterior to the trachea.
A small thyroid ima artery is present in approximately 10% of people; it ascends from the brachiocephalic trunk or the arch of the aorta to the isthmus of the thyroid gland.

The left brachiocephalic vein, jugular venous arch, and pleurae may be encountered, particularly in infants and children.
The thymus covers the inferior part of the trachea in infants and children.
The trachea is small, mobile, and soft in infants, making it easy to cut through its posterior wall and damage the esophagus.

A patient presents with hyperparathyroidism. He has a family history of his siblings having pituitary involvement, thyroid nodules, pancreatic involvement, parathyroid hyperplasia and cutaneous angiofibromas. Most likely diagnosis:
a. MEN 1
b. MEN 2A
c. MEN 2B
d. MEN 2C

Answer a. men1
3 p pancrease parathyroid and pituitary makes the diagnosis of men 1. I think no body will have doubt on that. Question is regarding thyroid nodule which may force us to make diagnosis of men2

Pheochromocytoma
This is a rare feature in MEN1. There have been fewer than 10 reported cases.[18] Most have been unilateral and chemically silent; one was malignant.[160] In two tumors, 11q13 loss of heterozygosity (LOH) was documented,[196] making it likely that all or most of these rare pheochromocytomas are true clonal expressions from biallelic MEN1 gene inactivation. This is supported by more frequent pheochromocytoma in a mouse model of MEN1.[59]

Thyroid Follicular Neoplasm
This has been associated with MEN1 since the earliest reviews. Although the association is probably correct, it is more likely related to the high incidence of thyroid follicular neoplasms in the general population (unrelated to MEN1) that are uncovered during the inevitable neck exploration for parathyroid disease in MEN1 than any causal association.[6] Further support for a coincidental association is the failure to identify MEN1 gene mutations in sporadic thyroid follicular tumors.[197]

Miscellaneous Nonendocrine Tumors
MEN1 has nonendocrine features that vary from rare to common, with some offering possible use in the diagnosis of MEN1.

Lipoma
This has been associated with MEN1 for over 30 years.[6] MEN1 lipomas are generally dermal, small, and sometimes multiple. Their frequency in MEN1 is about 30% versus 5% in control subjects without MEN1.[199] The frequency of lipomas in normal subjects has limited their use for MEN1 carrier ascertainment.

Multiple Facial Angiofibromas These have been found in 88% of MEN1 cases but not in control subjects.[199] Half of MEN1 cases have five or more. They are acneiform papules that do not regress and that may extend across the vermilion border of the lips (Fig. 36-7) .
Figure 36-7 Facial angiofibroma in patients with multiple endocrine neoplasia type 1. A small, light pink lesion on the vermilion border of the lip (top) and a large, reddish angiofibroma on the nose (bottom) are shown. Typical lesions are smaller and may require biopsy for confirmation. (From T. Darling and M. Turner, National Institutes of Health, Bethesda, Md.)

Collagenoma This was also observed in 72% of MEN1 cases but not in control subjects.[199] Collagenomas are whitish macular lesions about the trunk, sparing the face and neck. The MEN1 lipomas, angiofibromas, and collagenomas show loss of one copy of 11q13.[200] Thus, it is likely that these are clonal neoplasms and caused by inactivation of the (first and then) second copy of the MEN1 gene.

Spinal Cerebellar Ependymoma
This has been seen in four MEN1 cases.[18][201][202] There are no studies to determine whether 11q13 LOH or other MEN1 gene abnormalities are causative.

Malignant Melanoma
This has occurred in at least seven MEN1 cases, but direct involvement of the MEN1 gene has not been tested.[203]
Leiomyoma (of Esophagus, Lung, Rectum, or Uterus

A 30 year old man presents with 6 month history of nasal discharge, facial pain and fever. On antibiotic therapy, fever subsided. After 1 month again had symptoms of mucopurulent discharge from the middle meatus and the mucosa of the meatus appeared congested and oedematous. Next best investigation would be:
a. MRI of the brain
b. NCCT of the nose and para-nasal sinuses
c. Plain x-ray of the para-nasal sinuses
d. Inferior meatus puncture
Answer b NCCT of the nose and para-nasal sinuses

Computed tomography (CT) scanning is currently the method of choice for sinus imaging. Because a viral upper respiratory infection may cause abnormalities on CT that are indistinguishable from rhinosinusitis, imaging in acute bacterial rhinosinusitis has limited usefulness except when complications are suspected. On the other hand, symptoms of chronic rhinosinusitis do not correlate well with findings. Therefore, CT and/or nasal endoscopy is necessary to make the diagnosis. In addition to providing excellent visualization of mucosal thickening, air fluid levels, and bony structures, coronal scans give optimal visualization of the osteomeatal complex and are conveniently oriented for the surgeon in terms of surgical planning

196. A 40 year old man, smoker, complains of epigastric pain since an hour. On electrocardiographic examination he is found to have ST elevations suggesting an inferior wall infarction. Next step in the management would be:
a. Aspirin
b. Thrombolytic therapy
c. Pantoprazole
d. Beta-blockers

3-year old girl is posted for tonsillectomy. On examination it is found that she has a midline cystic swelling extending till below the hyoid bone. It is painless and moves with deglutition. The thyroid examination is normal. What should be done next?
a. Percutaneous aspiration
b. I.V. antibiotics c. Surgical removal
d. Observation

The surgery goes by the name, SISTRUNK's operation.

Thyroglossalcyst
This may be present in any part of the thyroglossal tract (Fig. 44.5). The common situations, in order of frequency, are beneath the hyoid, in the region of the thyroid cartilage, and above the hyoid bone. Such a cyst occupies the midline, except in the region of the thyroid cartilage, where the thyroglossal tract is pushed to one side, usually to the left. It is to be remembered that the swelling moves upwards on protrusion of the tongue as well as on swallowing because of the attachment of the tract to the foramen caecum.
A thyroglossal cyst should be excised because infection is inevitable, owing to the fact that the wall contains nodules of lymphatic tissue which communicate by lymphatics with the lymph nodes of the neck. An infected cyst is often mistaken for an abscess and incised, which is one way in which a thyroglossal fistula arises.

More than 60?mEq/L of chloride in sweat is diagnostic of CF when one or more other criteria are present. Threshold levels of 40?mEq/L for infants have been suggested. Values between 40 and 60?mEq/L suggest CF at all ages and have been reported in cases with typical involvement. In healthy adults, the sweat chloride values increase slightly, but a value of 60?mEq/L still adequately differentiates CF from other conditions. Chloride concentrations in sweat are somewhat lower in individuals who retain exocrine pancreatic function but remain within the diagnostic range. False-negative test results may be encountered in children with hypoproteinemic edema.

so here you can say that sweat chloride is normal

now read following lines

The finding of increased potential differences across nasal epithelium, the loss of this difference with topical amiloride application, and the absence of a voltage response to a ÃŸ-adrenergic agonist have been used to confirm the diagnosis in patients with equivocal or frankly normal sweat chloride values.

other refrence harrison 16th 1545 1546

Because of the large number of CF mutations, DNA analysis is not
used for primary diagnosis. The diagnosis of CF rests on a combination
of clinical criteria and analyses of sweat Cl values. The values for
the Na and Cl concentration in sweat vary with age, but typically
in adults a Cl concentration of 70 meq/L discriminates between
patients with CF and patients with other lung diseases.DNA analyses are being performed increasingly in patients with
CF. Comprehensive genotype-phenotype relationships have not yet
been established sufficiently for prognosis. A relationship between
F508 homozygosity and pancreatic insufficiency has been established,
but no predictive relationship holds for F508 homozygosity and lung
disease.]Between 1 and 2% of patients with the clinical syndrome of CF
have normal sweat Cl values. In most of these patients, the nasal
transepithelial potential difference is raised into the diagnostic range
for CF, and sweat acini do not secrete in response to injected -
adrenergic agonists.

so you can see that there no predictive value between 508 mutation and lung disease value and second thing they have clearly given potential differnce is the diagnostic test for normal sweat chloride test.

and 25 and 35 is normal range as you can see that it should be greater than 60.